telomerase inhibitors to treat hepatocellular carcinoma. They test their drugs on the purified telomerase from both humans and mice and find they are very potent inhibitors of enzyme activity. The drugs also inhibit growth of HEPG2 cells which are an immortalized human liver cell line. As a final study before commencing human trials, they test the effect of the drugs on formation of liver tumors in mice treated with a potent hepatocarcinogen. Unfortunately they see no effect of these drugs on development of liver tumors in mice. Explain the fundamental mistake the researchers made in this experiment. What defect might you expect these mice to have if their embryos were treated with these drugs early in development?

telomerase inhibitors to treat hepatocellular carcinoma. They test their drugs on the purified telomerase from both humans and mice and find they are very potent inhibitors of enzyme activity. The drugs also inhibit growth of HEPG2 cells which are an immortalized human liver cell line. As a final study before commencing human trials, they test the effect of the drugs on formation of liver tumors in mice treated with a potent hepatocarcinogen. Unfortunately they see no effect of these drugs on development of liver tumors in mice. Explain the fundamental mistake the researchers made in this experiment. What defect might you expect these mice to have if their embryos were treated with these drugs early in development?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter14: Biotechnology And Society

Section: Chapter Questions

Problem 13QP

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Similar questions

In 1994, telomerase activity was discovered in human cancer cell lines. Although telomerase is not active in human somatic tissue, human somatic cells do contain the genes for telomerase proteins and telomerase RNA. Since inappropriate activation of telomerase may contribute to cancer, why do you think the genes coding for this enzyme have been maintained in the human genome throughout evolution? Are there any types of human body cells where telomerase activation would be advantageous or even necessary? Explain.
In your own words, explain how cancer cells differ from normal cells in regard to the following: Telomeres, which are products of telomerase enzyme
You are interested in studying resistance to heavy metals and have selected the yeast Saccharomyces cerevisea to conduct your studies. You have recovered a deletion mutant that does not tolerate high concentrations of zinc (grows poorly in zinc containing media ) and have designated the mutant pgz-1 (for poor growth in zinc ). (a) What is the advantage to the type of mutant used in this work? What class of mutagen was likely use to generate pgz-1? ( b) Do you expect the PGZ gene to be expressed in your mutant? Explain.
Which of the following is true about the enzyme telomerase? A. It is found only in adult cells. B. It is responsible for telomere shortening. C. It can re-establish telomere length. D. It may speed up the aging process. E. It is expressed at low levels in cancer cells.
Mice that are engineered to block expression of the gene coding for telomerase protein age at a much faster rate than normal and have a decreased life span. The results of these mice experiments led researchers to propose that treatments that could lead to overexpression of the telomerase gene might serve as the “fountain of youth” leading to reversal of aging in humans. Why should we be very cautious about trying such treatments? Why it might be advantageous for multicellular organisms for most of their somatic cells not to express telomerase?
Why do adult human cells (other than germ cells and stem cells) NOT express the enzyme telomerase? In other words what benefit does not having telomerase provide to these cells?
In cancerous cells, telomeres are substantially longer then telomeres found in non-cancerous cells. As a result a number of scientists who study cancer treatment have become interested in telomerase. Why might telomerase be a good target for anticancer therapies? How might anticancer therapies targeting telomerase work (no need to design an experiment, just brainstorm how the therapy might impact telomeres of cancer cells)?
Telomerase is not active in most human cells. Some cancer biologists have suggested that activation of the telomerase gene would be a requirement for a cell to become cancerous. Explain why this might be the case.
Which type of mutation in telomerase is associated with cancer cells? a. Mutations that produce an inactive form of telomerase b. Mutations that decrease the expression of telomerase c. Mutations that increase the expression of telomerase d. All of the above
The experiment below is from a seminal set of experiments in the 1960s that illustrated the role of various repair pathways for DNA damage caused by UV radiation. In this experiment, the scientists isolated E coli strains that are mutant in the Rec A gene, the UvrA gene or both. They then irradiated cultures of each strain with increasing doses of UV light and measured the effect on cell viability. Answer the following questions about this data. A. Which DNA repair pathway and repair activity is inhibited by the Rec A mutant? B. Which DNA repair pathway and repair function is inhibited by UvrA mutant? C. Why is the UvrA/RecA double mutant so much more senitive to UV light than either mutant alone?
In the treatment of cancer, the basis for many types of chemotherapyand radiation therapy is that mutagens are more effective at killingdividing cells than nondividing cells. Explain why. What are possibleharmful side effects of chemotherapy and radiation therapy?
Budding yeasts such as S. cerevisiae exhibit telomerase activity throughout their life cycles, whereas human somatic cells do not exhibit telomerase activity. Suggest why this is so.